The renal response to exogenous parathyroid hormone in treated pseudohypoparathyroidism.

Resistance to the renal actions of parathyroid hormone (PTH) in pseudohypoparathyroidism (PsH) may be improved after treatment with vitamin D or its metabolites, but reports conflict. We have examined the renal response to infusion of 35 micrograms of 1-38 PTH in patients with PsH type I (n = 8) and PsH type II (n = 1) during treatment and related this to prevailing endogenous serum PTH and calcium levels. Nine patients with postsurgical or idiopathic hypoparathyroidism (HP) served as controls. The urinary cAMP increase (delta cAMP) was lower (p < 0.001) in the PsH type I (175 +/- 6.4 nmol/l glomerular filtrate) than in the HP group (3251 +/- 515 nmol/l glomerular filtrate). delta cAMP in the PsH type I subjects was dependent on endogenous PTH concentrations (r = -0.76; p = 0.046) and serum calcium (r = 0.74; p = 0.037). Phosphaturic responses (expressed as % decrease in TmPO4/glomerular filtration rate) were lower (p = 0.013) in the PsH type I (28.8 +/- 3.75) compared with those of the HP patients (43 +/- 3.48). The phosphaturic responses in the PsH type I patients were strongly dependent on endogenous PTH (r = 0.94; p < 0.001) and serum calcium levels (r = 0.94; p < 0.001) so that the responses of subjects with normal or low PTH levels were no different (p = 0.16) from the HP group. Renal handling of calcium and sodium in response to exogenous PTH was identical in patients with PsH (types I and II) and HP. Renal tubular reabsorption during a calcium infusion was normal in all patients with PsH. These results emphasise the importance of the modulatory effects due to associated biochemical abnormalities in PsH on the responses to exogenous PTH. They also confirm that renal handling of calcium and sodium is probably normal in treated PsH.

Comparison of low-dose intramuscular and intravenous salcatonin in the treatment of primary hyperparathyroidism.

The treatment of hypercalcaemia with low-dose salcatonin (100 U/d), administered either as a single intramuscular bolus or as a continuous intravenous infusion for five days, was examined in two groups of 10 patients with primary hyperparathyroidism, in a randomized open parallel study. Both the peak (0.31 +/- 0.035 mmol/L v 0.13 +/- 0.034 mmol/L) and overall (0.073 +/- 0.016 mmol/L v 0.018 +/- 0.016 mmol/L) hypocalcaemic responses were greater in the infusion group. The peak reduction in serum calcium occurred on day 2 of treatment after which there was a progressive attenuation of response. All the differences between the two methods of administration wer due to renal rather than bony effects of salcatonin. Possible causes of progressive resistance to treatment included reductions in sodium excretion and serum phosphate. It is concluded that low-dose salcatonin administered as a continuous infusion was more effective than the same dose given as a bolus. The kidney played a pivotal role both in the cause of the hypercalcaemia and in the response to treatment, including the rapid development of resistance which limits the use of salmon calcitonin in primary hyperparathyroidism to short-term reduction of serum calcium.